Congestive heart failure (CHF) is a condition that is often associated with a weakened heart that cannot pump enough blood to body organs. For example, as pumping action is lost, blood may back up into the heart and other areas of the body, including the liver, gastrointestinal tract, extremities and/or lungs. Implantable cardiac therapy devices are often used to overcome the deleterious effects caused by CHF, and in some cases to reverse the negative remodeling of the heart. Some implantable cardiac devices can also be programmed to compensate for worsening stages of CHF. For example, as CHF progresses, the myocardium weakens, which typically results in an increased left ventricular volume, also referred to as left ventricular dysfunction (LVD). To compensate for the increase in volume, a clinician may periodically measure a patient's left ventricular diameter, or another parameter associated with cardiac geometry, and program the implanted cardiac therapy device accordingly. This technique, however, requires clinical intervention, which consumes time and resources.
Some patients suffer from both congestive heart failure (CHF) and Cheyne-Stokes Respiration (CSR), which is defined as abnormal respiration in which periods of shallow/apneic breathing and deep breathing alternate (also known as periodic breathing). It has been found in studies that patients who suffer from both CHF and CSR tend to have larger left ventricular end-diastolic volumes (LVEDV), namely the volume of the left ventricle immediately prior to contraction of the left ventricle.
Lung and tissue gas stores of CO2 affect the rapidity of the CO2 exchange process from breathing, and thus have a direct influence on the respiratory control system damping. When the CO2 stores are relatively large, fluctuations in ventilation exert a smaller effect on alveolar and arterial PCO2 changes. Thus these gas stores act like a low-pass filter, attenuating the effect of rapid ventilatory fluctuations more than slow changes in ventilation.
As is well known, increased filling pressures (end-diastolic volume pressure) can lead to pulmonary vascular congestion and consequently, a decrease in pulmonary gas volume. This reduction in gas store will promote instability by elevating plant gain in the lung-chemoreflexor control. This gain is similar to hypercapnic ventilatory response slopes, which indicate the body's ability to expel CO2 following a period of hypoventilation (abnormally slow and shallow respiration), which results in hypercapnia (high levels of CO2 in the blood). It has also been discovered that hypercapnic ventilatory response among CHF patients with CSR is about double that compared to normal patients or those who suffer from obstructive sleep apnea.
What is needed is a reliable and convenient system and method that automatically determines progression and/or regression of heart failure, and that optionally can adjust patient therapy accordingly. Further, what is needed is a system that detects the rate at which CO2 is expelled, and which uses that rate to detect progression of CHF, and/or to identify patients with CHF who are also likely have CSR.